Immune-mediated demyelination.
Autor(es): Hartung H. P.
Resumo: The Guillain-Barré syndrome (GBS) and multiple sclerosis (MS) are thought to result from aberrant immune responses to myelin antigens. Recent evidence to implicate the cytokine tumor necrosis factor-alpha (TNF-alpha) and the intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of these disorders is reviewed. In GBS, elevated serum concentrations of TNF-alpha are detectable in 20 to 50% of patients. TNF-alpha released from autoreactive T cells, macrophages, or microglia may contribute to inflammatory demyelinative processes by upregulating the expression of recognition molecules on antigen-presenting cells; by cytotoxic damage to endothelium; by stimulating the secretion of inflammatory mediators; by directly injuring the myelin sheath; or by interfering with impulse propagation. Its pathogenic potential in GBS is underscored by findings in experimental autoimmune neuritis. Soluble ICAM-1, originating from T cells, macrophages, endothelium, or glial cells, circulates at increased concentrations in serum and cerebrospinal fluid of patients with active MS. ICAM-1 may be crucially involved in the migration of autoreactive T lymphocytes from blood to brain. Whether ICAM-1 can serve as a marker of acute inflammatory events in MS associated with clinical relapses warrants further investigation. TNF-alpha and ICAM-1 could be targets for antigen nonspecific treatment approaches to the inflammatory demyelinating diseases GBS and MS.
Imprenta: Annals of Neurology, v. 33, n. 6, p. 563-567, 1993
Identificador do objeto digital: 10.1002/ana.410330602
Descritores: Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Cytokines ; Guillain-Barre Syndrome - Immunology
Data de publicação: 1993
